Thus , we investigated the role of the PhoP-activated pagP and pgtE genes , because they had been implicated in resistance to the alpha-helical peptide C18G ( Guo et al. , 1998 ; Guina et al. , 2000 ) .
PhoP-suppressed genes include prgH and fliC [ 55 -- 57 ] , PhoP-activated genes include pmrAB , another two-component signal transduction system involved primarily in the protection of Salmo-nella to cationic antimicrobial peptides ( CAMP , see below ) [ 58 ] , mgtA and mgtCB encoding Mg transport 2 + systems , phoN , a periplasmic non-specific acid phospha-tase , pcgL encoding a periplasmic D-Ala -- D-Ala dipeptidase , or pagL , pagP and pgtE which contribute to increased resistance to CAMPs [ 59 -- 62 ] .
These regulated genes included induction of PhoP-activated genes ( pags ) pagCDPOK , virK , mgtBC , and pgtE , and repression of sopBD2 and the PhoP-repressed genes ( prgs ) prgHIJK .
These regulated genes included induction of PhoP-activated genes -LRB- pags -RRB- pgtE .